Integer topological defects offer a methodology to quantify and classify active cell monolayers

Monolayers of confluent elongated cells are frequently considered active nematics, featuring <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mo>±</mml:mo> <mml:mfrac><mml:mrow><mml:mn>1</mml:mn></mml:mrow> <mml:mrow><mml:mn>2</mml:mn></mml:mrow> </mml:mfrac> </mml:math> topological defects. In extensile systems, where cells extend further along their long axis, they can accumulate at <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mo>+</mml:mo> <mml:mfrac><mml:mrow><mml:mn>1</mml:mn></mml:mrow> <mml:mrow><mml:mn>2</mml:mn></mml:mrow> </mml:mfrac> </mml:math> defects and escape from <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mo>-</mml:mo> <mml:mfrac><mml:mrow><mml:mn>1</mml:mn></mml:mrow> <mml:mrow><mml:mn>2</mml:mn></mml:mrow> </mml:mfrac> </mml:math> defects. Nevertheless, collective dynamics surrounding integer defects remain insufficiently understood. We induce diverse + 1 topological defects (asters, spirals, and targets) within neural progenitor cell monolayers using microfabricated patterns. Remarkably, cells migrate toward the cores of all + 1 defects, challenging existing theories and conventional extensile/contractile dichotomy, which predicts escape from highly bent spirals and targets. By combining experiments and a continuum theory derived from a cell-level model, we identify previously overlooked nonlinear active forces driving this unexpected accumulation toward defect cores, providing a unified framework to explain cell behavior across defect types. Our findings establish + 1 defects as probes to uncover key nonlinear features of active nematics, offering a methodology to characterize and classify cell monolayers.